Hegde Shruti, Yesodharan Gemini, Tedrow John, Goldman Alena
Division of Cardiovascular Medicine, Department of Medicine, St. Elizabeth's Medical Center, Tufts University School of Medicine, USA.
Division of Pulmonary and Critical Care Medicine, Department of Medicine, St. Elizabeth's Medical Center, Tufts University School of Medicine, USA.
Case Rep Crit Care. 2020 Oct 28;2020:8875330. doi: 10.1155/2020/8875330. eCollection 2020.
Patients with severe COVID-19 pneumonia are hypercoagulable and are at risk for acute pulmonary embolism. Timely diagnosis is imperative for their prognosis and recovery. This case describes an otherwise healthy 55-year-old man with respiratory failure requiring mechanical ventilatory support secondary to COVID-19 pneumonia. Massive acute pulmonary embolism with right heart failure complicated his course.
A healthy 55-year-old man presented to our emergency department (ED) with a sore throat, cough, and myalgia. A nasopharyngeal swab was obtained, and he was discharged for home quarantine. His swab turned positive for SARS-CoV-2 infection on real-time reverse transcriptase-polymerase chain reaction assay (RT-PCR) on day 2 of his ED visit. A week later, he represented with worsening shortness of breath, requiring intubation for hypoxic respiratory failure due to COVID-19 pneumonia. Initially, he was easy to oxygenate, had no hemodynamic compromise, and was afebrile. On day 3, he became febrile and developed significant hemodynamic instability requiring maximum vasopressor support and oxygenation difficulty. His ECG revealed sinus tachycardia with S1Q3T3 pattern. On bedside TTE, there was evidence of right heart strain and elevated pulmonary artery systolic pressure of 45 mmHg. All data was indicative of a massive APE as the etiology for his hemodynamic collapse. A decision was made to forgo computed tomography pulmonary angiography (CTPA), given his clinical instability, and systemic thrombolytic therapy was administered. Within the next 12-24 hours, his hemodynamic status significantly improved.
This case highlights the importance of considering massive APE in COVID-19 patients as a cause of the sudden and rapid hemodynamic decline. Furthermore, timely diagnosis can be made to aid in appropriate management with the help of bedside TTE and ECG in cases where CTPA is not feasible secondary to the patient's hemodynamic instability.
重症新型冠状病毒肺炎（COVID-19）患者存在高凝状态，有发生急性肺栓塞的风险。及时诊断对其预后和康复至关重要。本病例描述了一名原本健康的55岁男性，因COVID-19肺炎导致呼吸衰竭，需要机械通气支持。他的病程中并发了大面积急性肺栓塞并伴有右心衰竭。
一名健康的55岁男性因咽痛、咳嗽和肌痛就诊于我院急诊科（ED）。采集了鼻咽拭子后，他被送回家中进行隔离。在急诊科就诊第2天，他的实时逆转录聚合酶链反应检测（RT-PCR）的拭子结果显示严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染呈阳性。一周后，他因COVID-19肺炎导致的低氧性呼吸衰竭，气短加重前来就诊，需要插管治疗。最初，他易于氧合，没有血流动力学障碍，也没有发热。在第3天，他开始发热，并出现明显的血流动力学不稳定，需要最大剂量的血管活性药物支持，且存在氧合困难。他的心电图显示窦性心动过速伴S1Q3T3图形。床旁经胸超声心动图（TTE）显示有右心劳损的证据，肺动脉收缩压升高至45 mmHg。所有数据均表明大面积急性肺栓塞是其血流动力学崩溃的病因。鉴于他的临床不稳定状态，决定不进行计算机断层扫描肺动脉造影（CTPA），而是给予全身溶栓治疗。在接下来的12至24小时内，他的血流动力学状态显著改善。
本病例强调了在COVID-19患者中考虑大面积急性肺栓塞作为突然和快速血流动力学下降原因的重要性。此外，在因患者血流动力学不稳定而无法进行CTPA的情况下，借助床旁TTE和心电图可及时做出诊断，以帮助进行适当的管理。
